# Drug Delivery Systems for Resiquimod to Control Myeloid‐Derived Suppressor Cells in Cancer Immunotherapy

## TL;DR

This paper reviews drug delivery systems for resiquimod to control MDSCs, which are key to improving cancer immunotherapy success.

## Contribution

The paper provides a focused review on optimizing drug delivery systems for resiquimod to target MDSCs in cancer immunotherapy.

## Key findings

- MDSCs are major contributors to immunotherapy failure and are important therapeutic targets.
- Resiquimod is highlighted as a promising drug candidate for controlling MDSCs.
- Optimized drug delivery systems are being explored to enhance the effectiveness of resiquimod.

## Abstract

Over the past decade, immunotherapy has emerged as the fourth pillar of cancer therapy, following surgery, chemotherapy, and radiotherapy. However, tumors often evade immune responses by altering the tumor microenvironment (TME), which recruits immunosuppressive cells such as myeloid‐derived suppressor cells (MDSCs), tumor‐associated macrophages, and regulatory T cells. Among these, MDSCs are considered key contributors to immunotherapy failure and have become major targets in new therapeutic strategies. Growing evidence indicates that controlling MDSCs is critical to the success of cancer immunotherapy, and several drug classes have shown feasibility. In this review, we introduce the significance of MDSCs as a target in cancer immunotherapy and highlight different therapeutic approaches to counteract their immunosuppressive functions. We discuss recent efforts to optimize drug delivery for controlling MDSCs, focusing on resiquimod (R848) as a representative drug candidate.

Myeloid‐derived suppressor cells (MDSCs) are key contributors to cancer immunotherapy failure and major targets in new therapeutic strategies. We highlight therapeutic approaches to counteract their immunosuppressive functions and discuss recent efforts to optimize drug delivery for controlling MDSCs, focusing on resiquimod as a representative drug candidate.